UK Parkinson's Disease Consortium - UKPDC
- Principal Investigators
- Research Groups
- Cell Physiology
- Clinical Neuroscience
- Clinical Studies
- Drosophila Genetics
- Molecular Biology and Biochemistry
- Molecular Neuropathology
- Neurological Biochemistry
- Neurological Signalling
- Protein Phosphorylation
- Contact us
Webcast of the presentation entitled ‘Advances in Genetic Understanding of Parkinson's Disease’ given by Nicholas Wood (University College London, United Kingdom) presented at the Biochemical Society Hot Topic event, PINK1-Parkin Signalling in Parkinson’s Disease and Beyond, held in December 2014. More...
A study published in Brain, led by researchers
at UCL Institute of Neurology, has shown that genetic mutations which
cause a decrease in dopamine
production in the brain and lead to a form of childhood-onset Dystonia,
also play a role in the development of Parkinson’s disease.
The new Leonard Wolfson Experimental Neurology Centre (LWENC) has opened for clinical studies and trials
In this paper Claudia Manzoni studies how fibroblast
cells from people with Parkinson’s disease caused by mutations in LRRK2
react to starvation. Although the changes are quite subtle, there are
differences between the way that fibroblasts that contain mutant LRRK2
respond to being starved – suggesting that there may be changes in the
way that these cells regulate a key process called autophagy (a term
which comes from the greek meaning to eat yourself, and is one of the
ways that cells get rid of waste and recycle proteins and organellles).
Research led by consortium researchers Dr Helene Plun-Favreau (UCL Institute of Neurology) and Dr Alex Whitworth (University of Sheffield), and collaborator Dr Heike Laman (University of Cambridge), has discovered how genetic mutations linked to Parkinson’s disease might play a key role in the death of brain cells, potentially paving the way for the development of more effective drug treatments. In the new study, published in Nature Neuroscience, the team of cross-institutional researchers showed how defects in the Parkinson’s gene Fbxo7 cause problems with mitophagy. More...
(MJFF Research Fellow)
I graduated in Pharmaceutical Biotechnology at the University of Milan and, to obtain my degree, I worked at the Mario Negri Institute for Pharmacological Research for 18 months on a project concerning the description of the synthetic peptide PrP82-146 as an in vitro model for prion amyloid. After graduation I remained at the Mario Negri Institute as research fellow in the lab. of Protein Chemistry and Biochemistry. In January 2006 I started my PhD with the Open University and I graduated in April 2010. For my PhD project I worked with Abeta amyloid investigating Abeta-induced neuronal toxicity and confirming that Abeta peptides, when appropriately folded, can impair neuronal viability following protein-mediated “docking” onto cell membranes. The aim of my study was to identify membrane proteins which might have a role in triggering Abeta-induced toxicity after binding to Abeta oligomers. In March 2010 I joined the Department of Molecular Neuroscience as associate research fellow under the supervision of Dr Patrick Lewis working on a project concerning the characterization of fibroblasts from PD patients with mutations in the LRRK2 protein, with specific interest for the mTOR and the TNFa signalling pathways.
|Link to Publications|
Page last modified on 13 aug 13 12:38